TY - JOUR
T1 - Propylthiouracil-induce hypothyroidism is associated with increased tolerance of the isolated rat heart to ischaemia-reperfusion
AU - Pantos, C.
AU - Malliopoulou, V.
AU - Mourouzis, I.
AU - Sfakianoudis, K.
AU - Tzeis, S.
AU - Doumba, P.
AU - Xinaris, C.
AU - Cokkinos, A. D.
AU - Carageorgiou, H.
AU - Varonos, D. D.
AU - Cokkinos, D. V.
PY - 2003/9/1
Y1 - 2003/9/1
N2 - The present study investigated the response of the hypothyroid heart to ischaemia-reperfusion. Hypothyroidism was induced in Wistar rats by oral administration of propylthiouracil (0.05%) for 3 weeks (HYPO rats), while normal animals (NORM) served as controls. Isolated hearts from NORM and HYPO animals were perfused in Langendorff mode and subjected to zero-flow global ischaemia followed by reperfusion (I/R). Post-ischaemic recovery of left ventricular developed pressure was expressed as % of the initial value (LVDP%). Basal expression of protein kinase C E (PKCE) and PKCδ and phosphorylation of p46 and p54 c-jun NH2-terminal kinases (JNKs) in response to I/R were assessed by Western blotting. LVDP% was found to be significantly higher in HYPO hearts than in NORM. At baseline, PKCE expression was 1.4-fold more in HYPO than in NORM hearts, P<0.05, while PKCδ was not changed. Furthermore, basal phospho-p54 and -p46 JNK levels were 2.2- and 2.6-fold more in HYPO than in NORM hearts, P<0.05. In response to I/R, in NORM hearts, phospho-p54 and -p46 JNK levels were 5.5- and 6.0-fold more as compared with the baseline values, P<0.05, while they were not significantly altered in HYPO hearts. HYPO hearts seem to display a phenotype of cardioprotection against ischaemia-reperfusion and this is associated with basal PKCE overexpression and attenuated JNK activation after I/R.
AB - The present study investigated the response of the hypothyroid heart to ischaemia-reperfusion. Hypothyroidism was induced in Wistar rats by oral administration of propylthiouracil (0.05%) for 3 weeks (HYPO rats), while normal animals (NORM) served as controls. Isolated hearts from NORM and HYPO animals were perfused in Langendorff mode and subjected to zero-flow global ischaemia followed by reperfusion (I/R). Post-ischaemic recovery of left ventricular developed pressure was expressed as % of the initial value (LVDP%). Basal expression of protein kinase C E (PKCE) and PKCδ and phosphorylation of p46 and p54 c-jun NH2-terminal kinases (JNKs) in response to I/R were assessed by Western blotting. LVDP% was found to be significantly higher in HYPO hearts than in NORM. At baseline, PKCE expression was 1.4-fold more in HYPO than in NORM hearts, P<0.05, while PKCδ was not changed. Furthermore, basal phospho-p54 and -p46 JNK levels were 2.2- and 2.6-fold more in HYPO than in NORM hearts, P<0.05. In response to I/R, in NORM hearts, phospho-p54 and -p46 JNK levels were 5.5- and 6.0-fold more as compared with the baseline values, P<0.05, while they were not significantly altered in HYPO hearts. HYPO hearts seem to display a phenotype of cardioprotection against ischaemia-reperfusion and this is associated with basal PKCE overexpression and attenuated JNK activation after I/R.
UR - https://www.scopus.com/pages/publications/0141507932
U2 - 10.1677/joe.0.1780427
DO - 10.1677/joe.0.1780427
M3 - Article
C2 - 12967335
AN - SCOPUS:0141507932
SN - 0022-0795
VL - 178
SP - 427
EP - 435
JO - Journal of Endocrinology
JF - Journal of Endocrinology
IS - 3
ER -
